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大肠杆菌ampC缺失突变体生长缺陷的互补作用

Complementation of growth defect in an ampC deletion mutant of Escherichia coli.

作者信息

Bishop R E, Weiner J H

机构信息

Department of Biochemistry, University of Alberta, Edmonton, Canada.

出版信息

FEMS Microbiol Lett. 1993 Dec 15;114(3):349-54. doi: 10.1111/j.1574-6968.1993.tb06597.x.

Abstract

beta-Lactamase genes of class-A (Rtem) and class-C (ampC) were placed under control of an inducible tac-promoter and expressed in Escherichia coli. Expression of RTEM had no observable effect on the growth properties of E. coli strains HB101 (ampC+) or MI1443 (delta ampC). E. coli MI1443 exhibited a decline in growth rate at mid-exponential phase which could be delayed by expression of AmpC at early-exponential phase. AmpC expression otherwise inhibited growth, particularly during the transition into exponential phase where growth was prevented altogether. We suggest that the AmpC beta-lactamase, but not RTEM, may have an additional cellular function as a peptidoglycan hydrolase.

摘要

A类(Rtem)和C类(ampC)β-内酰胺酶基因置于可诱导的tac启动子控制下,并在大肠杆菌中表达。RTEM的表达对大肠杆菌菌株HB101(ampC+)或MI1443(ΔampC)的生长特性没有可观察到的影响。大肠杆菌MI1443在指数生长期中期生长速率下降,而在指数生长期早期表达AmpC可延迟这种下降。否则,AmpC的表达会抑制生长,特别是在过渡到指数生长期时,此时生长会完全被阻止。我们认为,AmpCβ-内酰胺酶而非RTEM可能具有作为肽聚糖水解酶的额外细胞功能。

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